ANOMALY THREE: SELENIUM DEFICIENCY
A healthy person usually has between 800 and 1,200 CD4 T
lymphocytes (T-helper cells) in each cubic millimetre of their
blood. These lymphocytes play an essential role, signalling other
cells in the immune system to carry out their specific functions.
In the original conventional view of AIDS, it was believed that
HIV-1 directly killed CD4 T lymphocytes, so undermining the
immune system’s ability to function effectively. It is further
believed that when the CD4 T lymphocyte count falls below 200
per cubic millimetre, HIV-1 positive individuals become particularly vulnerable to the opportunistic infections such as tuberculosis, pneumocystis carinii pneumonia, and toxoplasmosis
and to the cancers that typify and are used to define AIDS.

When HIV-1 infection has been confirmed and AIDS is sus-pected, the number of CD4 T lymphocytes per cubic millimetre of a patient’s blood is regularly assessed as a guide to how well
the immune system is continuing to function. If the conventional model is correct and HIV is the sole cause of AIDS, it
would be logical to expect that this CD4 T lymphocyte count
would be the most accurate predictor of patient survival.14
It is
not. Plasma selenium levels are a far better indicator of the
probability of death from AIDS than are CD4 T lymphocyte
counts.
To illustrate, numerous studies have documented the presence of declining plasma selenium levels and an associated
decrease in glutathione peroxidase activity in individuals with
HIV/AIDS.15-17
More recently, Baum and co-workers18
have re-ported monitoring immunologic and nutritional factors at 6
month intervals, over 3.5 years, in 125 HIV-1-seropositive
drug-using men and women in Miami, Florida. This longitudinal study collected data on CD4 T lymphocyte count,
antiretroviral treatment, and plasma levels of vitamins A, E, B6, B12, and selenium and zinc. A total of 21 of the partici-pants died of HIV-related causes in the course of the study.
Only CD4 T lymphocyte counts over time (RR=0.69, p<0.04)
and selenium deficiency (RR=10.8, p<0.002) were significantly
associated with mortality, with selenium deficiency being the
superior indicator of it. Similarly, 24 HIV-infected children
were monitored for 5 years,19
during which time, 50 percent of
them died from HIV-related causes. In pediatric HIV-1 infection, as in adults, low plasma level of selenium was found to
be an independent predictor of mortality. Indeed, the lower
the serum selenium, the more rapidly death occurred, indicating that it was associated with faster disease progression.
In short, if one needs to predict whether or not a patient with
AIDS is likely to die, the best indicator of survival probability
is their plasma selenium level not their CD4 T lymphocyte
count. Why?”

„There seems to be more to the HIV-selenium relationship, how-ever, than just the depletion of this trace element by the virus.
Differences in environmental selenium levels appear to be influencing who is infected by HIV and where. This viewpoint is
now more accepted by the geochemists who study selenium.Indeed, the recently published Selenium World Atlas used the
incidence of HIV-positive populations as a surrogate measure
of selenium deficiency in Africa, since knowledge of actual soil
levels of this trace element is quite scarce.

This argument by analogy was made on the advice of E.W. Taylor, who was the
first to recognize that the diffusion of HIV-1 in Africa was occurring most rapidly in selenium deficient regions”

JAMA Pediatr. 2013;167(9):870-872. doi:10.1001/jamapediatrics.2013.108 Parenteral feedings containing more than 4 to 5 µg/kg/d of aluminum have been shown to result in neurodevelopmental delay in preterm infants.1 However, an infant at the 2-month checkup receives multiple aluminum-containing vaccines that in combination may have as high as 1225 µg of intramuscular aluminum; this is a much higher intramuscular aluminum dose than the safely recommended intravenous aluminum dose.2 Our first objective was to measure prevaccine and postvaccine levels of aluminum in preterm infants, a population at higher risk of aluminum neurotoxic effects
Results No significant change in levels of urinary or serum aluminum were seen after vaccination (Table). Significant declines were noted postvaccination in serum iron (58.1%), manganese (25.9%), selenium (9.5%), and zinc (36.4%) levels, as was a significant increase in serum copper level (8.0%). A rise in selenium level was the only significant urine change.

Significance
The results indicate that sub-chronic AlCl3 exposure caused the damage of the ovarian structure, the disturbed metabolism of Fe, Zn and Cu and the decreased activities of Na+–K+-ATPase, Mg2 +-ATPase and Ca2 +-ATPase in the ovary, which could result in suppressed energy supply in the ovary. A combination of suppression of energy supply and reduction of expression of FSHR and LHR could inhibit ovulation and corpus luteum development, leading to infertility in female rats. http://www.sciencedirect.com/science/article/pii/S0024320514002197
Aspects of aluminum toxicity. Hewitt C.D. – Savory J. – Wills M.R.
From: Clin Lab Med (1990 Jun) 10(2):403-22
Attention was first drawn to the potential role of aluminum as a toxic metal over 50 years ago, but was dismissed as a toxic agent as recently as 15 years ago. The accumulation of aluminum, in some patients with chronic renal failure, is associated with the development of toxic phenomena; dialysis encephalopathy, osteomalacic dialysis osteodystrophy, and an anemia. Aluminum accumulation also occurs in patients who are not on dialysis, predominantly infants and children with immature or impaired renal function. Aluminum has also been implicated as a toxic agent in the etiology of Alzheimer’s disease, Guamiam amyotrophic lateral sclerosis, and parkinsonism-dementia.

Abstract
Sepsis is characterized by severe redox imbalance. Glutathione plays a major role in cellular defenses against oxidative and nitrosative stress. There is limited information on the response of glutathione synthesis in human sepsis. This review proposes a critical analysis of available data on potential factors affecting glutathione synthesis in sepsis. Glutathione is synthesized from its constituent amino acids–glutamate, cysteine, and glycine. Cysteine availability and the activity of the enzyme glutamate cysteine ligase are rate-limiting for glutathione synthesis. Glutathione synthetic capacity is increased in liver and other tissues during the acute phase of experimental sepsis. Potential mechanisms for glutamate cysteine ligase activation in sepsis involve a decreased ratio of reduced/oxidized glutathione as well as the effects of reactive oxygen species, nitric oxide species, proinflammatory cytokines, heat shock proteins, and physical inactivity. Glutathione synthesis can be impaired by cysteine depletion, protein-energy malnutrition, hyperglycemia, glucocorticoid at pharmacologic doses, and decreased secretion of anterior pituitary hormones (growth hormones, thyrotropin, gonadotropins), as often observed in prolonged critical illness.

CONCLUSION:
The present finding suggested that type 1 DM patients were susceptible to oxidative stress and higher blood glucose level had an association with free-radical-mediated lipid peroxidation. Therefore, any means that can reduce oxidative stress may be beneficial for slow progression of cardiovascular complication in type 1 diabetic patients.

Journal of Toxicology
Volume 2011 (2011), Article ID 796719, 7 pageshttp://dx.doi.org/10.1155/2011/796719
Research Article
Cytotoxicity of Environmentally Relevant Concentrations of Aluminum in Murine Thymocytes and Lymphocytes
In humans, aluminum toxicity was first described as osteomalacic dialysis osteodystrophy [4]. Although aluminum has been primarily recognized as a neurotoxin and etiologic agent of dialysis dementia [5, 6], other detrimental health effects have been documented [7]. Some authors report aluminum-induced genotoxicity [8]. Others associate exposure to aluminum with osteodystrophy [9], anemia [10], and altered calcium homeostasis [11]. In addition, underlying conditions such as renal failure, leukemia, and diabetes increase aluminum retention in human and animal subjects due to impaired absorption and excretion, which in turn exacerbates its toxic effect [12, 13

Human exposure to aluminum other than during dialysis occurs primarily through ingestion of food and water, utilization of personal care products and cookware, and consumption of medications and administered vaccines [20–22]. Elevated levels of aluminum in soils have been implicated in the higher frequency of neurodegenerative disorders in the Kii Peninsula and natives in Guam [23

The injury observed in both thymocytes and lymphocytes was very rapid, occurring in some cases as quickly as measurements could be made. While the mechanism responsible is not clear, the speed of the injury suggests a direct effect on the plasma membrane. This action increases the permeability of the membrane to PI but does not result in total loss of membrane integrity over the period of time we have studied. We conclude that aluminum causes acute damage to the plasma membrane to a degree that allows some entry to PI, but not to such a degree that membrane integrity is completely lost. In acutely isolated cerebellar granule cells, aluminum has been found to cause a rapid neurotic cell death [34] while toxicity of cultured neurons has been reported to induce either apoptosis [35] or a combination of neurosis and apoptosis [36].

Two points are especially important. The concentrations of aluminum studied are environmentally relevant, being ones to which humans are commonly exposed. Secondly, the time course of cell damage was very quick, suggesting a direct damage to the thymocyte/lymphocyte plasma membrane. These results may be relevant to the study and understanding of the mechanism(s) of chronic exposure to low concentrations of aluminum, which may result in long latency and slow progression of disease [23]. In addition, alteration of plasma membrane integrity associated with exposure to aluminum could make cells more permeable to other unwanted substances. Given the prominence of aluminum in the environment and the susceptibility of thymocytes, further investigation of the effects of aluminum on immune system function is warranted.

Aluminium i DNA komórek grasicy

J Inorg Biochem. 2005 May;99(5):1145-54.
Thermodynamics of the interaction of aluminum ions with DNA: implications for the biological function of aluminum.

Wu J1, Du F, Zhang P, Khan IA, Chen J, Liang Y.
Abstract
Aluminum is a known neurotoxic agent and its neurotoxic effects may be due to its binding to DNA. However, the mechanism for the interaction of aluminum ions with DNA is not well understood. Here, we report the application of isothermal titration calorimetry (ITC), fluorescence spectroscopy, and UV spectroscopy to investigate the thermodynamics of the binding of aluminum ions to calf thymus DNA (CT DNA) under various pH and temperature conditions. The binding reaction is driven entirely by a large favorable entropy increase but with an unfavorable enthalpy increase in the pH range of 3.5-5.5 and at all temperatures examined. Aluminum ions show a strong and pH-dependent binding affinity to CT DNA, and a large positive molar heat capacity change for the binding, 1.57 kcal mol(-1) K(-1), demonstrates the burial of the polar surface of CT DNA upon groove binding. The fluorescence of ethidium bromide bound to CT DNA is quenched by aluminum ions in a dynamic way. Both Stern-Volmer quenching constant and the binding constant increase with the increase of the pH values, reaching a maximum at pH 4.5, and decline with further increasing the pH to 5.5. At pH 6.0 and 7.0, aluminum ions precipitate CT DNA completely and no binding of aluminum ions to CT DNA is observed by ITC. Combining the results from these three methods, we conclude that aluminum ions bind to CT DNA with high affinity through groove binding under aluminum toxicity pH conditions and precipitate CT DNA under physiological conditions.

Re: Polio eradication: a complex end game
Polio eradication by vaccination?
Let me quote some original seminal medical research.
Anderson et al. (1951) in his article “Poliomyelitis occurring after antigen injections” (Pediatrics; 7(6): 741-759) wrote “During the last year several investigators have reported the occurrence poliomyelitis within a few weeks after injection of some antigen. Martin in England noted 25 cases in which paralysis of as single limb occurred within 28 days of injection of antigen into that limb, and two cases following penicillin injections. In Australia, McCloskey, during a study of the 1949 outbreak, recorded 38 cases that developed within 30 days of an antigen injection, finding an association between the site of paralysis and that of the recently antecedent injection. His findings, contrary to Martin’s suggested a greater association with pertussis vaccine than with other antigens. Geffen, studying the 1949 poliomyelitis cases in London, observed 30 patients who had received an antigen within four weeks, noting also that the paralysis involved especially the extremity into which the injection had been given. In a subsequent survey of 33 administrative areas in England, Hill and Knowelden found 42 children who had been immunized within a month [of injections]…Banks and Beale3 observed 14 cases that followed within two months after immunization noting also a correlation between site of injection and location of paralysis, as well as increased severity of residual paralysis…In the discussion of this problem during the April 1950 meeting of the Royal Society of medicine, Burnett and others stressed the apparent relationship to multiple antigens containing a pertussis component”. [undoubtedly reflecting the increasing use of pertussis-containing vaccines].
Peterson et al. (1955) reported on vaccination induced poliomyelitis in Idaho as part of the trial of the Salk (injectable) vaccine (Vaccination-induced poliomyelitis in Idaho. Preliminary report of experience with Salk poliomyelitis vaccine. JAMA; 159 (4): 241-244).
The Cutter laboratories were accused of distributing vaccines containing live polioviruses, and singled out, even though vaccines produced by other manufacturers also caused paralysis (Nathanson and Langmuir 1963. The Cutter incident: poliomyelitis following formaldehyde-inactivated poliovirus vaccination in the United States during the spring of 1955 III. Am. J Hyg; 78: 61-81
Wyatt (1981) summarised cases of provocation poliomyelitis caused by multiple injections in his article “Provocation poliomyelitis: neglected clinical observations from 1914 to 1950” (Bull Hist Med; 55: 543-557).
Wyatt et al. (1992) and Wyatt (1993) warned against the unnecessary injections causing paralytic poliomyelitis in India (Trans Roy Soc Trop Med Hyg; 86: 546-549 and Lancet 341: 61-62, respectively).
Sutter et al. (1992) published an article “Attributable risk of DTP (Diphtheria and Tetanus toxoids and Pertussis toxoid vaccine injection in provoking paralytic poliomyelitis during a large outbreak in Oman”. (J Infec Dis; 165: 444-449).
According to Strebel et al. (1994. Paralytic poliomyelitis in Romania, 1984-1992. Am J Epidemiology; 140 (12: 111-124) ) although poliomyelitis due to wild virus had virtually disappeared from Romania (no cases reported between 1984-1989), the vaccine-associated paralytic poliomyelitis (VAPP) was reported at very high rates for over two decades. The overall risk of VAPP in Romania was up to 17 times higher than the reported risk in the USA.
In November 1990, to decrease the risk of VAPP, oral poliomyelitis vaccine produced in Romania was replaced by imported OPV produced by “Western European manufacturer”. However, the risk of PAPP continued unabated with that vaccine.
The history continued repeating itself all over the world wherever the poliomyelitis vaccines were used. Paralysis developed after both injectable and oral polio vaccines.
It comes as no surprise that the most recent mass polio vaccination programs fuelled by Bill and Melinda Gates Foundation resulted in increased cases of VAPP. In India, two paediatricians, Dr Neetu Vashisht and Dr Jacob Pulliel of the Department of Paediatrics of St Stephens Hospital in Delhi noted that another major ethical issue raised by the campaign is the failure to thoroughly investigate the increase in incidence “of non-polio acute flaccid paralysis (NPAFP)” in areas where many doses of vaccine were used, while noting that these cases are clinically indistinguishable from polio paralysis and twice as deadly.
They also noted that while India was declared polio-free in 2011, at the same time there were 47500 cases of NPAFP, which increased in direct proportion to the number of polio vaccine doses received. Independent studies showed that children identified with NPAFP “were at more than twice the risk of dying than those with wild polio infection”.
According to their report, nationally, the NPAFP rate is now twelve times higher than expected. In the states of Uttar Pradesh and Bihar – which have pulse polio vaccination every month – the NPAFP rate is 25 and 35 fold higher than the international norms (Ramesh Shankar, Mumbai 2012).
Ron Law (Assaulting alternative medicine: worthwhile or witch hunt? BMJ.com 10 March 2012) recently addressed the polio situation in India: eradication has been achieved by re-naming the disease. Poliomyelitis paralysis which occurs even after 30+ vaccination doses, is now called acute flaccid paralysis (AFP) or polio-like paralysis; hardly a great success of vaccination or comfort to the parents of the more than 60 000 affected children.
Earlier redefinition of poliomyelitis had been introduced in the US: a disease with residual paralysis which resolves within 60 days changed into a disease with residual paralysis which persists for more than 60 days. Cases of paralysis which resolve within 60 days (99% of cases) are diagnosed as viral or aseptic meningitis.
According to MMWR (1997; 32[29]: 384-385), there are 30 000 to 50 000 cases of viral/aseptic meningitis per year in the US. Considering that in the pre-vaccine era the vast majority (99%) of the reported cases were non-paralytic (corresponding to aseptic or viral meningitis), vaccination has actually increased the incidence of poliomyelitis. Before mass vaccination there were a few hundred or few thousand cases of polio in some outbreaks, while now it is up to 50 000 cases every year.
Figure 1 in Schonberger et al. (1984. Control of poliomyelitis in the United States. Rev infect dis; 6 (Suppl 2: S424-S426) shows the steady downward trend in the incidence of poliomyelitis stopping, and indeed increasing, when DPT and P vaccination became mandatory in the US in the mid-seventies.
The experience in northern Namibia showed that with no polio vaccination children developed natural immunity to the wild polio virus without developing paralysis (Biellik et al. 1994. Poliomyelitis in Namibia. Lancet 344: 1776).
The vaccine viruses inactivation by a 14-day treatment with 1:4000 formaldehyde solution is the subject to asymptotic factor making the inactivation incomplete (Gerber et al. 1961. Inactivation of vacuolating virus (SV 40) by formaldehyde, Proc Soc Exp Biol & Med; 108: 205-209), and, Fenner (1962. The reactivation of animal viruses. BMJ; July 21: 135-142) showed that the process is also reversible.
Evans et al. (1985. Nature ; 314: 548-550) demonstrated “Increased neurovirulence associated with a single nucleotide change in a noncoding region of the Sabin type 3 poliovirus genome”.
The only way to eradicate paralytic poliomyelitis is to stop vaccinating.http://www.bmj.com/content/344/bmj.e2398/rr/578260http://szczepienie.blogspot.com/p/polio-poliomyelitis-opv-opw-porazenia.htmlhttps://szczepieniapolio.wordpress.com/ofiary-szczepien-doustnych-wirusem-polio-typu-3-w-polsce/http://szczepienia.wybudzeni.com/2016/12/14/historia-poliomyelitis/

Abstract
The scope of the work was to investigate the influence of selenate fertilisation and the addition of symbiotic fungi (mycorrhiza) to soil on selenium and selenium species concentrations in garlic. The selenium species were extracted from garlic cultivated in experimental plots by proteolytic enzymes, which ensured liberation of selenium species contained in peptides or proteins. Separate extractions using an aqueous solution of enzyme-deactivating hydroxylamine hydrochloride counteracted the possible degradation of labile selenium species by enzymes (such as alliinase) that occur naturally in garlic. The selenium content in garlic, which was analysed by ICP-MS, showed that addition of mycorrhiza to the natural soil increased the selenium uptake by garlic tenfold to 15 microg g(-1) (dry mass). Fertilisation with selenate and addition of mycorrhiza strongly increased the selenium content in garlic to around one part per thousand. The parallel analysis of the sample extracts by cation exchange and reversed-phase HPLC with ICP-MS detection showed that gamma-glutamyl-Se-methyl-selenocysteine amounted to 2/3, whereas methylselenocysteine, selenomethionine and selenate each amounted to a few percent of the total chromatographed selenium in all garlic samples. Se-allyl-selenocysteine and Se-propyl-selenocysteine, which are selenium analogues of biologically active sulfur-containing amino acids known to occur in garlic, were searched for but not detected in any of the extracts. The amendment of soil by mycorrhiza and/or by selenate increased the content of selenium but not the distribution of detected selenium species in garlic. Finally, the use of two-dimensional HPLC (size exclusion followed by reversed-phase) allowed the structural characterisation of gamma-glutamyl-Se-methyl-selenocysteine and gamma-glutamyl-Se-methyl-selenomethionine in isolated chromatographic fractions by quadrupole time-of-flight mass spectrometry.